Inim3003 - Challenges Facing Microbial Resistance To Antibiotics (Bacterial Pathogenicity)

Front 1

What is a biofilm?

Back 1

An example of a community i.e. a collection of bacteria occupying the same physical habitat.

Front 2

What comprises an biofilm?

Back 2

Exopolysaccharides form a fibrous capsule that create a sporadic biolayer with spaces for food to enter and waste to leave

Front 3

Pilli in biofilm formation

Back 3

Assist adherence by identifying human epithelium at mucosal surface

Front 4

Where do biofilms develop most rapidly

Back 4

Flowing systems where adequate nutrients are available e.g. mucosal systems.

Front 5

What is quorum sensing

Back 5

Ability of bacterial cells to communicate with each other inducing a particular response at a particular moment in time

Front 6

What is an autoinducer

Back 6

Small molecule that mediates quorum sensing e.g. a homoserine lactone

Front 7

Autoinducers - low cell densities

Back 7

Diffuses away from cell

Front 8

Autoinducer - high cell density

Back 8

Accumulation and reaching level sufficient to activate gene transcription

Front 9

Property of a biofilm - 1

Back 9

Metabolism and cell division slow down

Front 10

Property of a biofilm - 2

Back 10

Production of ECM

Front 11

Property of a biofilm - 3

Back 11

Antibiotic resistance and resistance vs host both increase. This is due to sharing of bacterial DNA between bacterial within a biofilm

Front 12

Property of a biofilm - 4

Back 12

One bacteria can contribute to a state of resistance that can help a whole community

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Biofilm steps of development - 1

Back 13

Attachment

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Biofilm steps of development - 2

Back 14

Extracellular exopolysaccharide matrix produced

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Biofilm steps of development - 3

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Early biofilm architecture

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Biofilm steps of development - 4

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Shedding of bacterial cells from biofilm

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Bacterial pathogenicity - capsule

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Produces biofilm matrix and also helps with evasion of phagocytosis.

Is normally harmless unless there is a break in the endothelium facilitating spread.

Front 18

Bacterial pathogenicity - LPS

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O-antigen on surface mimics human cell surface therefore providing immune evasion

Lipid A (that tethers O-antigen to bacteria) causes septic shock.

Front 19

Invasins - hyaluronidase

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Produced by staph, strep and clostridium (i.e. all gram positive)

Breaks down connective tissue by degrading hyaluronic acid.

Front 20

Invasins - collagenase

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Produced by C. histolyticum and C. pefingens.

Breaks down collagen and can lead to gas gangrene.

Front 21

Invasins - neuraminidase

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Produced by vibrio cholerae and shigella dysenteriae.

Cleaves neuraminic (sialic) acid found on epithelial cells within intestinal mucosa.

Front 22

Invasins - streptokinases and staphylokinase

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Produced by strep and staph respectively

Convert inactive plasminogen to plasmin and act to break down fibrin in blood clots. This leads to rapid diffusion of infectious bacteria

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Host cell damage - C. perfingens

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Phospholipases - target phospholipids in cell membrane by removal of polar heads

Lecithinases - target lecithin in cell membrane

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Host cell damage - haemolysins

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Alpha toxin (staph) and streptolysin (strep).

May be channel forming proteins, phospholipases or lecithinases that form pores in RBCs (and phagocytes) causing cell death due to necrotic imbalances.

Front 25

Coagulase

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Diffusible enzyme associated with staph a (and almost never staph epidermis) that converts fibrinogen

By clotting, fibrin could also provide an antigenic disguise thereby assisting bacteria in evading the host immune system

Front 26

Extracellular digestive enzymes

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Lipases, proteases, glycohydrolases etc

Do not have a role in pathogenesis but may have a role in nutrition/metabolism etc